Worldwide, 40% of children, 33% of male non-smokers, and 35% of female non-smokers were exposed to second-hand smoke in 2004 ⁷, This exposure was estimated to have caused 379 000 deaths from ischemic heart disease and a total of 603 000 premature deaths, 47% of which occurred in women, 28% in children, and 26% in men. Disability adjusted life years lost because of exposure to SHS amounted to 10.9 million, of which 61% were in children. The largest disease burdens in adults (2 836 000) were from ischemic heart disease ⁷ Prospective cohort studies showed high risks of SHS for coronary heart disease ⁸ and stroke ⁹, without evidence of a threshold ¹⁰. Especially at work places like bars or discotheques, where many smokers release SHS, substantial increases of acute coronary events were found ^{11, 12}. The acute cardiovascular effects of SHS were attributed mainly to the ultrafine particles released from the burning end of cigarettes between puffs ^{11, 13}.

Chronic inhalation of SHS contributes to development of CVD in healthy persons by oxidative stress and vascular inflammation, while acute effects of SHS are triggering manifestation of CVD in risk groups ^{11, 14, 15}. Toxins distributed on the large surface of ultrafine particles inhaled with SHS elicit acute endothelial dysfunction with inactivation of nitric oxide (mediating vasodilatation), impairment of the viability of endothelial cells and reduction of the number and functional activity of circulating endothelial progenitor cells. In addition, platelets of non-smokers appear to be susceptible to pro-aggregatory changes with every passive smoke exposure. Apart from vasoconstriction and thrombus formation from sticky platelets, increased fibrinogen and other factors of blood coagulation, the myocardial oxygen balance is further impaired by SHS-induced adrenergic stimulation and autonomic dysfunction with heart rhythm disturbances ^{11, 15, 16, 17} and impairments of diastolic function ¹⁸. Experiments in healthy men showed that a 30 minute exposure to SHS (e.g. the time of a meal) is sufficient for reduction of coronary flow velocity reserve ¹⁹ and sustained vascular injury characterized by mobilization of dysfunctional endothelial progenitor cells with blocked nitric oxide production and triggering of platelet aggregation in blood ^{15, 16, 20, 21}. Chronic vascular effects of SHS start with endothelial dysfunction in children ²², arterial stiffness ²³ and develop to thickening of intima-media ²⁴ and atherosclerosis ^{25, 26}. Combined effects of tobacco smoke with ambient air pollution have been detected ²⁷, so that interactions have to be assumed also for SHS and ambient PM2.5. Complex interactions with nutrition are likely, especially in connection with diabetes. SHS is a risk factor for metabolic syndrome ^{28, 29}, glucose intolerance ³⁰, insulin resistance and the development of type 2 diabetes mellitus ³¹. A meta-analysis of 6 prospective cohort studies ³² concluded, that SHS increases the relative risk of new diabetes to 1.21 (95 % CI 1.07–1.38). Another meta-analysis on 7 prospective studies ³¹ found that the increase of the relative risk for developing type 2 diabetes from passive smoking was 1.33 (95% CI 1.20-1.46) and after adjustments for publication bias it was 1.27 (95%CI 1.16-1.40). After manifestation of diabetes vascular complications are increased by exposure to tobacco smoke.

Most at risk for acute effects of SHS like myocardial infarction or stroke are patients with preexisting coronary or cerebrovascular diseases, which in turn are promoted by chronic exposure to SHS. Since Sargent et al. ³³ published reduced incidence of admissions for myocardial infarction associated with a public smoking ban, numerous studies confirmed, that enforcement of smoke-free laws rapidly reduces admissions for acute coronary syndrome ^{34, 35, 36} and also other cardiac and cerebrovascular diseases ³⁷. Smoke-free legislation is associated with a lower risk of hospitalization and death from CVD, significantly lower rates of hospital admissions or deaths from coronary events (relative risk, 0.85; 95%CI 0.82–0.88), other heart disease (relative risk, 0.61; 95%CI 0.44–0.85),and cerebrovascular accidents (relative risk, 0.84; 95%CI 0.75–0.94). More comprehensive laws were associated with larger changes in risk ³⁷. Indoor smoking bans reduced myocardial infarction up to 33-40% ^{33, 38} and in most studies by 10-20%, in the first year mainly associated with the elimination of passive smoking and followed by sustainable decreases of coronary syndrome, myocardial infarction, stroke and incident diabetes also in ex-smokers ^{37, 39, 40, 41, 42}. With a smoke-free hospitality industry people recognized tobacco smoke as an air pollutant, smoking in public was denormalized and social acceptance of smoking in front of children and pregnant women decreased also in homes and in cars ^{43, 44, 45, 46, 47}. A meta-analysis came to the conclusion that public smoking bans (workplaces including the hospitality industry) reduced children’s exposure to SHS at home by 28% ⁴⁸. Therefore it is not surprising that enforcement of smoke-free legislation was also followed by a 10% reduction in preterm birth and hospital admissions of children with asthma ⁴⁹.

Substantial and rapid reaction of the cardiovascular system (platelet and endothelial function, arterial stiffness, atherosclerosis, oxidative stress, inflammation, heart rate variability, energy metabolism, and increased infarct size) explains why SHS increases the risk of coronary heart disease by about 30% ⁵⁰. Cardiovascular risks have been underestimated in many studies by comparison of active smokers with non-smokers, of which a large part was exposed to SHS ⁵¹. There is evidence of a strong, consistent and dose-dependent association between exposure to secondhand smoke and risk of myocardial infarction and stroke, suggestive of a causal relationship, with disproportionately high risk at low levels of exposure suggesting no safe lower limit of exposure for risk groups ^{10, 11}. Chronic exposure of persons, which are healthy at beginning of exposure, is associated with a continuous increase of risk of CVD over the years. Already Whincup et al. ⁵² were able to show, that in male, light and heavy passive smokers, classified by serum cotinine at beginning of follow up, major coronary heart disease increased by years of follow up. The increase in heavy passive smokers was comparable to the increase in light active smokers. In a European cohort a hazard ratio of 1.25 (95%CI 1.04-1.50) was calculated for passive smoking (verified in a subsample by plasma cotinine) per each additional daily hour of exposure ⁵³. A meta-analysis on health effects of SHS found a relative risk of 1.35 (95 % CI: 1.22-1.50) for stroke and 1.27 (95 % CI: 1.10-1.48) for ischemic heart disease ⁵⁴. The risks were higher in women. Flores et al. ⁵⁵ proved that the premature mortality hazard of recalled and unconscious exposure to SHS is comparable and predicted by serum cotinine at beginning of observation. There was a significant trend in years of life lost, adjusted for confounders, across cotinine categories both in non-smokers (P < 0.0001) and non-smokers reporting no SHS exposure (P = 0.002).

The younger the child the more vulnerable it seems to be, especially for SHS effects on brain and lungs, but also CVD ^{56, 57}. Recently a meta-analysis on parental smoking and the risk of congenital heart defects concluded, that maternal active smoking was significantly associated with risk of atrial septal defect and right ventricular outflow tract obstruction and that also maternal passive smoking as well as paternal smoking increased the risk of congenital heart defects in offspring ⁵⁸. Many effects of prenatal exposure to tobacco smoke have been attributed to nicotine ⁵⁹, with adverse perinatal outcomes associated to placental syndromes ⁶⁰ and direct toxic effects on arteries supplying the fetus ^{61, 62} and his heart ^{63, 64}. Prenatal exposure to constituents of tobacco smoke can also have long lasting effects on children and only few epidemiological studies were able to disentangle them from effects of postnatal exposure ^{65, 66}.

SHS leaves accumulating contaminants on surfaces like carpets, wallpapers, upholstery, blankets or soft toys and these remnants endanger in particular children by oral, dermal and inhalation uptake from house dust, etc.. Even parents omitting contamination of indoor air nevertheless bring toxins and carcinogens to indoor spaces and to their children by clothes, hair, skin and breath, but the highest contamination is found on surfaces of rooms used for smoking. From these surfaces toxins are released back into the air and by aging and chemical transformations more toxic pollutants are formed, e.g. residual nicotine from tobacco smoke sorbed to indoor surfaces reacts with ambient nitrous acid to form carcinogenic nitrosamines ^{67, 68, 69}. Animal experiments demonstrated numerous effects of THS: hyperactivity, persistent changes in the immune and hematopoietic system, lung cancer, liver damage, increased thrombogenesis, and metabolic effects, including elevated triglycerides, increased LDL, decreased HDL, and insulin resistance through oxidative stress ^{69, 70, 71, 72}. Estimates of harm from THS are all by inference, since direct evidence of human health problems arising from THS is not available.

Cardiovascular Risks of Passive Exposure to Emissions of Water Pipe, Heated Tobacco and Electronic Cigarettes

Water pipe (shisha) produces similar risks for bystanders as tobacco cigarettes, but concentrations of carbon monoxide and heavy metals are higher in SHS from shisha. Depending on intensity and duration of passive exposure similar CVDs could develop as proven for active consumption, while acute cardiovascular effects on risk groups are expected mainly from fine particulate matter, carbon monoxide and nicotine ^{73, 74, 75}. Animal experiments showed hypercoagulability, inflammation, as well as systemic and cardiac oxidative stress ⁷⁶.

Heated tobacco products (HTPs) are marketed as less dangerous than conventional cigarettes because of less products of pyrolysis, however, biomarkers of potential cardiovascular harm did not support this claim ⁷⁷. HTPs impair vascular endothelial function measured by arterial flow-mediated dilatation in rats to the same extent as by cigarette smoke ⁷⁸. An advantage of electronic devices over conventional cigarettes is that SHS is only produced when the user exhales the aerosols and not continuously like in conventional smoking released from the burning end of cigarettes between puffs. The doses calculated for SHS uptake from electronic devices were significantly lower, below 1.6×108particles/kg bodyweight, than those due to combustion devices, but dosimetry estimates were 50% to 110% higher for HTPs than for e-cigarettes ⁷⁹. The carrier function of aerosols from e-cigarettes might be similar, but the clearance of liquid particles is certainly faster than of solid particles released by conventional cigarettes. On the other hand, harmful volatile organic compounds, tobacco-specific nitrosamines and heavy metals in electronic cigarettes can be even higher in e-cigarettes than in traditional cigarettes ⁸⁰.

Electronic cigarettes have been called “wolf in sheep’s clothing”, because they may serve as a gateway drug for youth, prolong nicotine addiction and the ritual in smokers who would otherwise be willing to quit and keep up the handling and use of cigarettes in public ⁸¹. Exposure of bystanders to products of pyrolysis are lower than in passive smoking, but exposure to nicotine is similar and particles in the aerosol are smaller ^{82, 83, 84, 85}. Aerosols exhaled during vaping are less persistent than SHS, nevertheless they are carriers for toxins, which they adsorb on their large surface and transport them into the depth of the lung, where clearance is less efficient ⁸¹. Contamination of neighboring rooms was found ⁸⁶ and it has to be assumed that also passive vaping increases cardiovascular risks, which were found for active vaping ^{87, 88}. Though exposure to nano-particles is not as high as in passive exposure to heated tobacco, the combination of ultrafine particles with nicotine and other toxins has to be regarded as a respiratory ⁸⁹ and cardiovascular risk, which is avoidable ⁹⁰. For smoking cessation dermal and oral nicotine products from pharmacies are safer for nicotine replacement and do not contaminate the breathing air of bystanders ⁸¹. Most worrying are associations found recently between e-cigarette use and myocardial infarction ⁹¹.